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Mediators of Inflammation
Volume 2014, Article ID 902038, 10 pages
Review Article

Trypanosoma cruzi Infection and Host Lipid Metabolism

1National Reference Centre for Parasitology, Research Institute of McGill University Health Centre, Montreal General Hospital, Montreal, QC, Canada H3G 1A4
2Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada H3A 2B4

Received 26 April 2014; Accepted 5 August 2014; Published 3 September 2014

Academic Editor: Marcelo T. Bozza

Copyright © 2014 Qianqian Miao and Momar Ndao. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Trypanosoma cruzi is the causative agent of Chagas disease. Approximately 8 million people are thought to be affected worldwide. Several players in host lipid metabolism have been implicated in T. cruzi-host interactions in recent research, including macrophages, adipocytes, low density lipoprotein (LDL), low density lipoprotein receptor (LDLR), and high density lipoprotein (HDL). All of these factors are required to maintain host lipid homeostasis and are intricately connected via several metabolic pathways. We reviewed the interaction of T. cruzi with each of the relevant host components, in order to further understand the roles of host lipid metabolism in T. cruzi infection. This review sheds light on the potential impact of T. cruzi infection on the status of host lipid homeostasis.